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Peptic ulcer.pdf
Peptic Ulcer Disease
Definition
‘’Condition in which there is a discontinuity
in the entire thickness of the gastric or
duodenal mucosa that persists as a result
of acid and pepsin in the gastric juice’’
•The term peptic ulcer applies to mucosal
ulceration near the acid bearing regions of
GIT.
•Peptic ulcer disease (PUD) = Mucosal
defect in the GIT (gastric or duodenal)
exposed to acid and pepsin secretion.
Disease Prevalence
• Lifetime Prevalence = 10% of Americans
develop PUD.
• 10% of GERD patients with abdominal
pain diagnosed with PUD.
• Prevalence decreasing over last 30yrs.
• Male-to-female ratio of gastritis = 1:1
• Male-to-female ratio of PUD = 2:1
Gastric Ulcer
•
•
•
•
•
Epigastric pain occurring 30
minutes to 1 hour after meals.
Aggravated by eating
(because acid secretion
increase at meal time) leads to
weight loss.
Relieved by vomiting (because
acid is expelled out).
No pain at hours of sleep (HCL
production decreases at hours
of sleep).
More common in persons older
than age 50.
•
•
•
•
•
Duodenal Ulcer
Epigastric pain occurring 2-3
hours after meals.
Relieved by food (because the
pyloric sphincter, at the
junction of stomach and
duodenum, closes upon eating
to concentrate food in the
stomach) causes weight gain.
Not relived.
Pain at hours of sleep
(because gastric emptying
continuous at hours of sleep).
More common between age 25
and 50.
Ad

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Peptic ulcer.pdf

  • 4. Definition ‘’Condition in which there is a discontinuity in the entire thickness of the gastric or duodenal mucosa that persists as a result of acid and pepsin in the gastric juice’’ •The term peptic ulcer applies to mucosal ulceration near the acid bearing regions of GIT. •Peptic ulcer disease (PUD) = Mucosal defect in the GIT (gastric or duodenal) exposed to acid and pepsin secretion.
  • 5. Disease Prevalence • Lifetime Prevalence = 10% of Americans develop PUD. • 10% of GERD patients with abdominal pain diagnosed with PUD. • Prevalence decreasing over last 30yrs. • Male-to-female ratio of gastritis = 1:1 • Male-to-female ratio of PUD = 2:1
  • 6. Gastric Ulcer • • • • • Epigastric pain occurring 30 minutes to 1 hour after meals. Aggravated by eating (because acid secretion increase at meal time) leads to weight loss. Relieved by vomiting (because acid is expelled out). No pain at hours of sleep (HCL production decreases at hours of sleep). More common in persons older than age 50. • • • • • Duodenal Ulcer Epigastric pain occurring 2-3 hours after meals. Relieved by food (because the pyloric sphincter, at the junction of stomach and duodenum, closes upon eating to concentrate food in the stomach) causes weight gain. Not relived. Pain at hours of sleep (because gastric emptying continuous at hours of sleep). More common between age 25 and 50.
  • 8. • PUD develop only in presence of acid environment. • Excess of gastric acid is not necessary for ulcer development. • Person with a gastric ulcer has normal to less than normal gastric acidity compared with person with a duodenal ulcer. • Some intraluminal acid does seem to be essential for a gastric ulcer to occur.
  • 9. Dyspepsia • Dyspepsia is defined as persistent or recurrent pain or discomfort centered in the upper abdomen • Peptic ulcer presents as dyspepsia • Not all patients with dyspepsia have PUD • Most common causes of dyspepsia are non-ulcer or GERD and peptic ulcer. • Other causes include gastric cancer, pancreatic or biliary disease
  • 10. Etiology and Pathophysiology • Pepsinogen is activated to pepsin in presence of HCl and a pH of 2 to 3. • Secretion of HCl by parietal cells has a pH of 0.8. • pH reaches 2 to 3 after mixing with stomach contents. • Surface mucosa of stomach is renewed about every 3 days. • Mucosa can continually repair itself except in extreme instances.
  • 11. Etiology and Pathophysiology • Mucosal barrier prevents back diffusion of acid from gastric lumen through mucosal layers to underlying tissue. • Mucosal barrier can be impaired and back diffusion can occur. • HCL freely enters mucosa when barrier is broken • Result: –Injury to tissue occurs –cellular destruction and inflammation
  • 13. Disruption of Gastric Mucosal Barrier
  • 15. • H.pylori • NSAIDs (even at low dose) • Coffee/Caffeine • Ethanol • Tobacco • Severe physiologic stress (Burns, CNS trauma, Surgery, Severe medical illness) • Steroids Common Risk Factors.
  • 16. Symptoms • • Abdominal pain is the most common symptom of the Peptic Ulcer. Other possible symptoms include: – Nausea – vomiting – Weight loss – Fatigue – Heartburn – indigestion – Chest pain – Blood in vomiting – Bloody or dark tarry stools
  • 17. Common form of PUD 1: H-PYLORI associated ulcer. 2: NSAIDs associated ulcer. 3: STRESS ulcer.
  • 18. Helicobacter pylori • Gram –ve microaerophillic bacterium found in gastric antrum of human stomach. • 95% duodonal ulcer and 80% of gastric ulcers are associated with H.pylori. • The effect of H.pylori in patients receiving NSAIDs is unclear.
  • 19. Helicobacter pylori's initiation of mucosal inflammation
  • 20. Mechanism of H-pylori • • • To avoid the acidic environment of the interior of the stomach H-pylori uses its flagella to burrow into the mucus lining of the stomach to reach the epithelial cells where there is a more neutral pH. H. pylori is able to move towards the less acidic region ( chemotaxis). H. pylori is found in the mucus on the inner surface of the epithelium and occasionally inside the epithelial cells themselves. It adheres to the epithelial cells by producing adhesins which bind to lipids and carbohydrates in the epithelial cell membrane.
  • 21. Mechanism of H-pylori • H. pylori causing peptic ulcer disease may be more virulent than in those without ulcers • It produces cytotoxin associated gene A proteins and vacuolating cytotoxins such as vac A, which activate the infalmmatory cascade • Gene A and vac A are the predictors of the ulcerogenic capacity of the strain
  • 22. Mechanism of H.pylori • Gastrin conc. is also increased in H.pylori infection which causes hypergastrinaemia • High acid content in the proximal duodenum leads to metaplastic gastric- type mucosa, which provides a place for H. pylori infection followed by inflammation and ulcer formation
  • 23. Mechanism of H-pylori • H. pylori also neutralizes the acid in its environment. It does this by producing large amounts of urease which breaks down the urea present in the stomach to carbon dioxide and ammonia. •
  • 24. Discovery of Helicobacter pylori • “Two Australian physicians won the 2005 Nobel Prize in Medicine or Physiology for showing - at least partly by accident -- that many ulcers are the result of a bacterial infection.” “Robin Warren and Barry Marshall's work on ulcers was pioneering”
  • 25. NSAIDs • Approximately 15% of patients on long-term NSAID develop PUD. • NSAIDs - ↓prostaglandin (PG) by inhibiting the cyclooxygenase (COX) enzymes. • Three iso-enzymes COX-1, COX-2, COX-3 • COX-1 → PG production in gastric mucosa.
  • 26. NSAIDs associated ulcer • NSAID induced peptic ulcers are the ulcers in stomach or first part of doudenum which are associated with the intake of Non-steroidal anti- inflammatory drugs. • Patients with Rheumatide Arthritis Osteoarthritis taking NSAIDs have an and ulcer incidence of approximately 15-20%. • The overall risk for serious adverse GI events in patients taking NSAIDs is about three times greater than that of controls. • In elderly patients (>60), this risk rises to 4-5 times than that of control.
  • 27. Prevention • • Patients at high risk for hemorrhage and perforation from aspirin and other NSAID- induced ulcers should be considered for prophylaxis with misoprostol. Proton pump inhibitors are an acceptable alternative for prevention of NSAID-related complications.
  • 28. Treatment of NSAID induced Ulcer • The medications may include one or more of the following: – Antibiotics to kill Helicobacter pylori. – H2 blockers (like Famotidine (Zepsin), Ranitidine, or Cimetidine). – Proton pump inhibitors (such as Omeprazole) – Medications that protect the tissue lining (like Sucralfate). – Bismuth (may help protect the lining and kill the bacteria).
  • 29. Differentiating between H.pylori and NSAID-induced ulcer H. Pylori • more often in duodenum. • Often superficial. • less severe GI bleeding. • More symptomatic. NSAIDs • more often in stomach. • often deep. • more severe GI bleeding. • sometimes asymptomatic
  • 30. Other Disease Conditions Associated with PUD • Hypersecretory states: Gastrinoma (Zollinger-Ellison syndrome) or multiple endocrine neoplasia (MEN-I). • Diseases associated with increased risk of PUD: cirrhosis, chronic pulmonary disease, renal failure.
  • 32. Physical Exam Findings In uncomplicated PUD exam findings few and non-specific: • Epigastric tenderness - usually mild. • Bowel sounds - normal. • Signs of peritonitis with perforation.
  • 34. Lab Studies to Evaluate PUD • CBC - evaluate acute/chronic blood loss. • H. Pylori - Serologic antibody test for HP – does not determine if active HP infection. - Fecal antigen test for active HP. - Urea breath test for active HP.
  • 35. Principles in Selecting H.Pylori Test Based on the following: • Probability of previously eradicated infection. • Probability of current active infection. • Need to document active infection. • Need for rapid result. • Patient preferences. • Cost (both of test and possible unnecessary treatment).
  • 36. When is a Serology Test Useful? Not useful in • Populations with low disease prevalence. • Elderly populations to detect active disease. Useful in • Patients who never received H. pylori treatment. • Symptomatic patients not using NSAIDs.
  • 37. H. Pylori Stool Antigen (HpSa) Test • Useful in initial diagnosis + confirmation of eradication. • Sensitivity of 91% and a specificity of 92%. • Test requires collection of stool sample. • Performed in lab. • Requires little preparation, however patients may not be compliant with collecting sample.
  • 39. Urea Breath Test • Useful for initial diagnosis + confirmation of eradication. • Sensitivity and specificity over 90%. • Urease activity is present in the stomach in those infected with H pylori. • Ingest urea labeled with radioactive carbon. • Hydrolysis of urea → labeled carbon dioxide (CO2) • Rapidly absorbed into bloodstream and within a few minutes, appears in breath.
  • 41. Breath Test Compared to HpSa • Requires more patient preparation. • More expensive. • Number of drugs can adversely affect accuracy . • Antibiotics and bismuth → stop for 4 weeks. • Proton pump inhibitors → stop for 7 days. • Patients need to fast for at least 6 hours. • Breath test cannot be used in pregnant women.
  • 43. Imaging Studies • Chest x-ray if perforation is suspected to detect free abdominal air. • Upper gastrointestinal series – Performed by experienced radiologist is close to diagnostic accuracy of endoscopy. – Not as sensitive as endoscopy in diagnosis of small ulcers (<0.5 cm). – Unable to obtain biopsy to rule out malignancy.
  • 45. Endoscopy Endoscopy indicated in following high risk patients: • >50 years old with new-onset dyspepsia. • Dyspepsia with dysphasia(speech disorder) and weight loss. • Evidence of GI bleeding. • Failed appropriate trial of empiric therapy. • Using NSAIDs or other high risk medicines. • Signs of UGI tract obstruction (vomiting). • Ethnic background associated with increased risk UGI malignancies. Endoscopy
  • 48. Over the Counter Remedies • Aluminum and magnesium hydroxide salt (Maalox®, Mylanta®) Neutralizes gastric acidity. • Aluminum side effect = constipation • Magnesium side effect = diarrhea • Magnesium and aluminum mixtures used to avoid side effects.
  • 49. • Calcium Carbonate (Tums®, Rolaids®) – calcium salt neutralizes acid. • Bismuth subsalicylate (Pepto-Bismol®) – binds to ulcer base forming a protective coat, has anti-inflammatory and bactericidal properties.
  • 50. H2-Blockers • Selectively block H2-receptors on parietal cells reducing acid secretion . • Used primarily in ulcer disease not associated with H pylori. • Treatment duration is 6-8 week.
  • 51. Side Effects of Cimetidine/Tagamet® • Elderly patients – confusion • Young males - impotence • May alter levels of other drug - warfarin, TCA’s, triamterene, phenytoin, propranolol, metronidazole, anti-arrythmics. • May alter renal function so requiring lower doses.
  • 52. Proton Pump Inhibitors • Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump. • Relieve pain and heal peptic ulcers more rapidly than H2 blockers. • Drugs in this class are equally effective. • Four weeks to treat active PUD.
  • 54. Other Pharmacotherapy Agents • Sucralfate (Carafate®) Binds proteins in exudates and forms a viscous adhesive that protects GI lining. • Misoprostol (Cytotec®) Prostaglandin analog- protects lining of GI tract by replacing depleted prostaglandin E1. Prevents peptic ulcers in patients taking NSAIDs.
  • 56. H. Pylori Triple Therapy Treatment • Triple therapy for 14 days is treatment of choice. • Two forms of triple therapy: PPI–based and bismuth-based. • PPI based = PPI + 2 antibiotics for 2 week & continue PPI for additional 2 weeks. • Bismuth based = bismuth subsalicylate + 2 antibiotics for 2 weeks with addition of H2- blocker to optimize ulcer healing.
  • 57. H Pylori Treatment Side Effect Rating Cure Rate medium 80-90% medium-low 80-90% medium 80-90% Three Drug Regimens Clarithromycin500mg + Metronidazole500mg BD + PPI 20- 40mg Amoxicillin1g + Clarithromycin 500mg + PPI 20-40mg Amoxicillin 1gm + Metronidazole 500mg + PPI 20-40mg Combination Products
  • 58. Type Drug Selected Side Effects Comments Antacids Aluminum hydroxide Calcium carbonate Magnesium hydroxide Sodium bicarbonate Nausea, headache, weakness, loss of appetite, constipation (aluminum hydroxide) or diarrhea (magnesium hydroxide) Used mainly to relieve symptoms, not as a cure Histamine-2 blockers •Cimetidine •Famotidine •Nizatidine •Ranitidine Rash, fever, muscle pains; may cause breast enlargement and erectile dysfunction in men; may interfere with elimination of certain drugs (cimetidine); confusion (cimetidine, ranitidine) The once-daily dose is taken in the evening or at bedtime; doses taken in the morning are less effective Proton pump inhibitors •Lansoprazole •Omeprazole •Pantoprazole •Rabeprazole •Esomeprazole Diarrhea, constipation, headache Usually well tolerated; most effective means of reducing stomach acid Antibiotics •Amoxicillin •Clarithromycin •Metronidazole •Tetracycline Diarrhea (amoxicillin, clarithromycin, tetracycline), altered taste, nausea Effective for treating peptic ulcers caused by Helicobacter pylori infection Miscellaneous Bismuth subsalicylate •Misoprostol •Sucralfate Diarrhea (bismuth subsalicylate, misoprostol); darkening of the tongue and stool (bismuth subsalicylate); spontaneous abortion (misoprostol); constipation (bismuth subsalicylate); may reduce effectiveness of other drugs (sucralfate) Bismuth subsalicylate is used in combination with antibiotics to cure H. pylori infection
  • 60. PUD Complications • Hemorrhagic shock from a perforated ulcer. • Symptomatic relief with PPI may mask symptoms of gastric malignancy. • Gastritis may present as bleeding, more likely in elderly. • Symptoms of anemia (fatigue, dyspnea).
  • 61. Initial Treatment Plan in the Absence of High Risk Symptoms Based on current evidence, no single strategy has been demonstrated to be more medically effective than any other. • Empiric therapy with acid suppression. • Empiric H pylori testing and treating strategy. • Early endoscopy.
  • 62. Final Recommendations • Alarm symptoms = endoscopy. • No alarm symptoms = medical management favored approach. • Studies still in progress to evaluate if medical management versus endoscopy is both medically and cost effective in long-term. • Lack of response or the recurrence of symptoms warrants endoscopy.
  • 63. Medical Legal Pitfalls • Failure to consider non-GI cause of epigastric pain. • Failure to consider GI bleed in absence of abdominal pain (especially in elderly). • Lack of follow-up care resulting in failure to diagnose gastric cancer. • Failure to recommend endoscopy early in high risk patients. • Failure to obtain a history regarding NSAID use.
  • 64. References: oClinical Pharmacy and Therapeutics by Roger Walker. oPharmacology by Lippon cott. oClinical and Disease Management by Dr. Inam Danish. oPharmacotherapy Hand Book.